Objective To investigate the protective effect of emodin on hippocampal neural cells in mice with epilepsy induced by kainic acid. Methods A total of 90 male ICR mice were randomly divided into control group, status epilepticus (SE) group, and emodin treatment groups (at doses of 100, 200, and 400 mg/kg), with 18 mice in each group. Kainic acid was used to establish a mouse model of SE. HE staining and TUNEL staining were used to observe the effect of emodin on the morphological changes and apoptosis of hippocampal neural cells in mice with epilepsy; colorimetry was used to measure the content of glutathione (GSH) and malondialdehyde (MDA) and the activity of superoxide dismutase (SOD); RT-PCR and Western blot were used to measure the mRNA and protein expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and caspase-3. Results Emodin (200 and 400 mg/kg) significantly alleviated the injury and apoptosis of hippocampal neural cells induced by epilepsy, increased the activities of GSH and SOD, and reduced the activity of MDA (P<0.05). It also reduced the mRNA and protein expression of IL-1β, TNF-α, and caspase-3 in the hippocampus (P<0.05). Conclusions Emodin has antioxidant, anti-inflammatory, and anti-apoptotic effects on hippocampal neural cells in mice after SE, possibly by increasing the activities of GSH and SOD, reducing the content of MDA, and inhibiting the expression of IL-1β, TNF-α, and caspase-3.